The system of multiplication of the coccidios, with alternation between phases sexuadas and sexless, allows a single ooquiste, which is the unit infecting mature, producing tens of thousands of intermediate forms with remarkable activity enteropathica.

The pathology of coccidiosis must be understood from two ways:

Clinic:

Sudden and progressive onset of the disease, leading to mortality and highly characteristic symptoms in each species of coccidia and type of bird.

 Subclinical:

When the infection does not get to have entity as to cause symptoms, either because the number of coccidios is low, or because there are factors that are immune to interfere with the progress of the infestation.

The pathogenicity of the different Eimeria species varies according to the strain and the number of oocysts sporulated ingested in a given time, their capacity for multiplication, the genetic susceptibility of the birds receiving, of the possible existence of immunity, density and general conditions of hygiene of the exploitation.

The impact of coccidiosis is primarily focused on contributing to worse feed conversion, slow growth, increase mortality and decrease significantly the normal performance of the farms.

When the infection is severe, the birds appear lethargic, their plumage is dull and lackluster, and they may experience excessive drooling, low appetite, and—in the case of certain coccidial infections—diarrhea, depigmentation, etc.

The eimeria or coccidia that can affect animals are:

Causing serious problems:

E. acervulina. E. Mivati E. máxima. E. necatrix. E. Brunetti, E. Tenella.

Of little significance:

E. praecox. E. mitix. E. hagani.

Each species presents as a feature that has a specific demarcation of settlement in the digestive tract.

Ingestion of a single ooquiste:

If the bird is responsive, you can delete it after a few days hundreds of thousands of oocysts, destroying many other cells of the organism.

The period of sporulation is the time that elapses between a ooquiste is expelled through the feces until it becomes infective.

In terms of illness, it would not be proper to single out the coccidiosis, as there are several ways quite different, depending on the species affecting the birds.

The coccidios have a similar development, but pathogenically are very different.

Coccidia always enter birds through the oral route, when one or more infectious sporulated oocysts are ingested.

The oocysts are the primary forms excreted by the feces of the animals parasitized. As in latent form, can live for many months, because:

• They can survive in the external environment for up to a year at temperatures between 0 °C and 30 °C.
• They are resistant to solar radiation, drought, and humidity.
• Temperatures of 80–90 °C destroy them in a matter of seconds.
• At a temperature of 60 °C, they survive for only twenty minutes.
• Antiseptics do not affect them, making them very difficult to eliminate with conventional chemical disinfectants.

The coccidios are protozoa microscopic present a system of development and reproduction in the breast of other living cells, acting as an intracellular parasite.

The development of the coccidios on the host:

It has two phases:

The one from propagation or stage of schizogony.

The one from reproduction or phase of gametogonia, which determines its great development and dissemination.

When oocysts are expelled in the feces, they have a large, central nucleus; this form is not infectious, as the oocyst must first sporulate in the external environment (exogenous phase).

In this stage, the nucleus divides twice, forming four sporocytes, each of which contains two sporocytes; in other words, a single oocyst produces eight infective sporocytes, which remain active within the coccidian membrane.

This sporulation process takes between 12 and 30 hours, depending on the species, and requires suitable environmental conditions—including temperature, oxygen, and humidity—otherwise the oocyst will not develop.

The infection of birds occurs in the moment that the oocysts sporulated are ingested.

Then begins the phase of endogenous, which takes place in the digestive tract, where they are released esporócitos and the sporozoites by the action of the digestive juices.

Although the released sporozoites primarily affect digestive cells (enterocytes), they also enter the bloodstream.

The sporozoites penetrate the enterocytes, where they develop, increase in size, and transform into merozoites I. Within these merozoites, the so-called first-generation schizonts I form—falciform, highly abundant, and motile structures—which then go on to infect other cells.

The schizonts passed on to other cells (enterocytes) develop a globose form called merozoite II, which in turn form another generation of schizonts II, which are released to the lumen of the gut after the corresponding cytopathic effect.

The cycle can be repeated once more, but in the end it exhausts the capacity of multiplying asexually, called esquizogónica, in which case the schizonts evolve with sexual dimorphism, forming macrogametocitos or microgametocitos, and this new phase is called gametogonia.

The release of motile microgametocytes is the step preceding the fertilization of macrogametocytes. Once fertilization has occurred, a zygote forms and the macrogametocyte’s membrane thickens; once released into the intestinal lumen, it will develop into an oocyst, which will be expelled in the feces, thus completing the coccidian life cycle.

The course of the disease and its severity depend largely on the age of the animals when they contract it.

In order to make the study of coccidiosis, there's that cater to the diverse parasitic forms, since each species of Eimeria presents some distinct features: